Renal fibrosis: not just PAI-1 in the sky.

Fogo AB
J Clin Invest. 2003 112 (3): 326-8

PMID: 12897200 · PMCID: PMC166301 · DOI:10.1172/JCI19375

A delicate balance exists between ECM synthesis and degradation such that interruption of the corresponding pathways results in increased plasminogen activator inhibitor-1 (PAI-1), pathological matrix accumulation, and glomerulosclerosis. A new study demonstrates that therapy with a mutant PAI-1 increases matrix turnover and reduces glomerulosclerosis by competing with endogenous PAI-1, suggesting therapeutic utility in the treatment of fibrotic renal disease.

MeSH Terms (13)

Animals Cell Movement Extracellular Matrix Fibrosis Humans Kidney Kidney Diseases Macrophages Mice Mice, Knockout Mutation Plasminogen Activator Inhibitor 1 Rats

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